It is now generally accepted that the light dark cycle is the most important environmental stimulus for entraining circadian rhythms in most species, including humans. The unexpectedly large magnitude of the phase shifts we have observed after cyclic bright light exposure indicates that human subjects are capable of a strong (Winfree's Type O) resetting response to bright light, and suggests that the responsiveness of the human circadian pacemaker to light is within the wide range of sensitivity observed in lower organisms. Yet, in every organism for which strong (Type O) resetting has been found experimentally, a stimulus of reduced strength has been shown to induce weak (Winfree's Type 1) resetting. Characterization of the relationship between stimulus strength and the topology of circadian phase resetting by light in humans is critical to understanding how the human circadian pacemaker responds to environmental light exposure. Based on our preliminary data, three testable hypotheses are proposed: (1) a single 5-hour exposure to bright light can reset the circadian pacemaker by an amount which is dependent on the initial circadian phase of the light exposure; (2) the strength of the resetting response to bright light is dependent on the number of stimulus cycles; (3) there is a n on-linear relationship between he strength of the resetting response to bright light and the continuity of the light stimulus. To test these hypotheses a series of experiments are proposed utilizing methodologies that allow direct measurement of circadian phase both before and after exposure to bright light. The phase-response curves to a single- cycle, two-cycle, and three-cycle bright light stimulus will be determined tin human subjects to test the hypotheses that a 3-cycle bright light stimulus produces strong (Type O) resetting, whereas a stimulus of reduced strength produces weak Type 1 resetting. Finally, the resetting response to an interrupted bright light stimulus will be analyzed to test the hypothesis that bright light initiates its phase-shifting effect on the pacemaker more rapidly when the light exposure begins than it decays when the light exposure ends. This work has significant implications for the treatment of circadian rhythm disorders, such as delayed-sleep phase syndrome, advanced-sleep phase syndrome, shift-work dyssomnia and jet-lag. Careful analysis of the effects of a single exposure to bright light exposure or of interrupted bright light episodes have important implications for the practical applications of bright light treatment for circadian rhythm sleep disorders, since repetitive uninterrupted exposure to bright light for many hours and days is often not feasible in a clinical or occupational setting.